Preadaptations

[Phronesis]

It still doesn't answer my question of how preadaptation is (at a gross level) distinuishable from neutral mutations becoming benificial due to a change in enviroment as described by the hypothesis of puntuated equilibrium.

Could you please explain why you think preadaptation is indistinguishable from a neutral mutation becoming beneficial due to a change in environment. There are two things I do not get.

Firstly, a neutral mutation that occurs in a functional protein has no effect on the protein with regards to fitness. For example:
Carboxylesterase X is able to break down carboxylesters with short acyl chains in catalytic domain Y. A neutral mutation will have no effect (or little effect) on the ability of carboxylesterase X to degrade carboxylesters with short acyl chains. Also, neutral mutations are often silent mutations. A shift in environment change, say to a nylon rich environment, won't alter its original function. However, if the protein is able to break down the nylon (in catalytic domain Y), it has been coopted into a new function while retaining its old function, and neutral mutations did not have much (if anything) to do with it. Carboxylesterase X could be argued to be a preadaptation for nylon break down, even though neutral mutations did not contribute much with regards to the evolution of catalytic domain Y and its ability to break down nylon. Sure, neutral mutations play a role in evolution, but preadaptations are not necessarily neutral mutations and neutral mutations are not necessarily preadaptations.

Secondly (from the talkorigins site),

Gould and Eldredge did not specify any particular genetic mechanism for PE.

Thus, I am confused where you gt this:

It still doesn't answer my question of how preadaptation is (at a gross level) distinuishable from neutral mutations becoming benificial due to a change in enviroment as described by the hypothesis of puntuated equilibrium.

Please explain.

I'm not quite sure what all the fuss is about then, it's really nothing more than glorified natural selection finding niches to exploit and occassionally causing speciation.

The fuss is (or so the scientists say) is the surprising degree of complexity at the base of the tree. The fuss is that the cells which gave rise to plants and animals had more types of genes available to them than are presently found in either plants or animals. The fuss is the unexpected find of building blocks for nerves in animals at the base of the tree. Interesting don't you think . And there are a LOT more interesting things to discuss.

And I know you do actually find this to be interesting :

It's a flattened blob (Tricoplax), a few millimeters across and made up of a few thousand cells. It's main claim to fame is its remarkable simplicity: it is a multicellular animal that consists of only four apparent cell types, and the only obvious organization is into an upper and lower surface. The upper surface consists of a sheet of covering cells, while the lower surface contains two cell types: the gland cells that secrete digestive enzymes onto whatever the animal is sitting on, and the cylinder cells that absorb whatever nutrients are released. In between is a loose network of fiber cells that are responsible for the animal's movement.

One other strange thing: in culture, Trichoplax is consistently asexual and reproduces by fission, but older cultures at high density begin to produce small motile presumptive sperm cells, and as individual animals desintegrate, they spew out ova. The two have never been observed to come together, though, so there is no fertilization, and while the ova may divide a half dozen times, they all eventually die. It is possible that there is another stage in the life cycle that is not viable under laboratory conditions and has never been observed.

 

[Phronesis]

More Trichoplax preadaptations:

The Dlx gene​

What does it do (wiki)?

• Dlx genes are required for the tangential migration of interneurons from the subpallium to the pallium during vertebrate brain development [3].
  
• It has been suggested that Dlx promotes the migration of interneurons by repressing a set of proteins that are normally expressed in terminally differentiated neurons and act to promote the outgrowth of dendrites and axons [4]. Mice lacking Dlx1 exhibit electrophysiological and histological evidence consistent with delayed-onset epilepsy [5].
  
• Dlx2 has been associated with a number of areas including development of the zona limitans intrathalamica and the prethalamus.
  
• Dlx5/6 expression is necessary for normal lower jaw patterning in vertebrates [6].
  
• Dlx7 is expressed in bone marrow

A quick BLAST of the sequence reveals it is closely related to human Dlx1, as well as Dlx1 in other vertebrates (including Zebrafish, the mouse, rat opossum, dog etc.)

More specifically, what does Dlx1 do?
Pubmed

This gene encodes a member of a homeobox transcription factor gene family similiar to the Drosophila distal-less gene. The encoded protein is localized to the nucleus where it may function as a transcriptional regulator of signals from multiple TGF-{beta} superfamily members. The encoded protein may play a role in the control of craniofacial patterning and the differentiation and survival of inhibitory neurons in the forebrain. This gene is located in a tail-to-tail configuration with another member of the family on the long arm of chromosome 2. Alternatively spliced transcript variants encoding different isoforms have been described.

It is possible to create a homology of this protein to look at its possible structure. The closest match is the human Dlx 5 protein structure. Sequence alignment places the Dlx sequence of Trichoplax closer to human Dlx5 than to human Dlx1 (Figure 1: ClustalW - original settings).
What does Dlx 5 do?
Pubmed:

This gene encodes a member of a homeobox transcription factor gene family similar to the Drosophila distal-less gene. The encoded protein may play a role in bone development and fracture healing. Mutation in this gene, which is located in a tail-to-tail configuration with another member of the family on the long arm of chromosome 7, may be associated with split-hand/split-foot malformation.

The homology model of the protein:
A good quality protein was generated (Figure 2: Swissmodel)

So, a Hox gene responsible for a sundry of neurologically associated developmental processes present in an organism with no nerve, sensory or bone cells at the base of the evolutionary tree.
Awesome .​

 

[alloytoo]

Could you please explain why you think preadaptation is indistinguishable from a neutral mutation becoming beneficial due to a change in environment. There are two things I do not get.


Firstly, a neutral mutation that occurs in a functional protein has no effect on the protein with regards to fitness. For example:
Carboxylesterase X is able to break down carboxylesters with short acyl chains in catalytic domain Y. A neutral mutation will have no effect (or little effect) on the ability of carboxylesterase X to degrade carboxylesters with short acyl chains. Also, neutral mutations are often silent mutations. A shift in environment change, say to a nylon rich environment, won't alter its original function. However, if the protein is able to break down the nylon (in catalytic domain Y), it has been coopted into a new function while retaining its old function, and neutral mutations did not have much (if anything) to do with it. Carboxylesterase X could be argued to be a preadaptation for nylon break down, even though neutral mutations did not contribute much with regards to the evolution of catalytic domain Y and its ability to break down nylon. Sure, neutral mutations play a role in evolution, but preadaptations are not necessarily neutral mutations and neutral mutations are not necessarily preadaptations.

Stop cutting and pasting, own words please.

At a gross level:

Adaptation occurs (through whatever mechanism).

For example, hairs modified into defensive quills are then modified into noise-making rattles.

It's glorified natural selection.

The fuss is (or so the scientists say) is the surprising degree of complexity at the base of the tree. The fuss is that the cells which gave rise to plants and animals had more types of genes available to them than are presently found in either plants or animals. The fuss is the unexpected find of building blocks for nerves in animals at the base of the tree. Interesting don't you think . And there are a LOT more interesting things to discuss.

And I know you do actually find this to be interesting :

Again at a gross level, it's nothing more than glorified natural selection.

 

[Phronesis]

Stop cutting and pasting, own words please.

Now you are just scraping the bottom. Am I not to use my own words now all of a sudden?

At a gross level:

Adaptation occurs (through whatever mechanism).

For example, hairs modified into defensive quills are then modified into noise-making rattles.

It's glorified natural selection.

Could you please explain in a little more detail please. I am sorry, I really am unable to grasp what you are trying to convey here.

Again at a gross level, it's nothing more than glorified natural selection.

Again, could you please elaborate a bit more when you allude to "gross level"? I am missing something here.

 

[alloytoo]

Now you are just scraping the bottom. Am I not to use my own words now all of a sudden?

Ok one line summary. Go boy go.

Could you please explain in a little more detail please. I am sorry, I really am unable to grasp what you are trying to convey here.

Again, could you please elaborate a bit more when you allude to "gross level"? I am missing something here.

Unpreadapted=naturally unselected

it's not difficult to grasp.

 

[Phronesis]

Ok one line summary. Go boy go.

Sorry, it can't get simpler than that, you are going to have to read and understand that bit for yourself.

Unpreadapted=naturally unselected

it's not difficult to grasp.

Unpreadapted? Naturally unselected? Again, I am sorry, but you are going to have to elaborate here. New terms, new ideas, how do these terms fit into the picture?

A Hox gene responsible for a sundry of neurologically associated developmental processes present in an organism with no nerve, sensory or bone cells at the base of the evolutionary tree. Nice hey .

 

[alloytoo]

A Hox gene responsible for a sundry of neurologically associated developmental processes present in an organism with no nerve, sensory or bone cells at the base of the evolutionary tree. Nice hey .

Nice hey?

This is the point of the thread. Kewl hey!

 

[Phronesis]

Awesome, I am humbled by your fascination with preadaptations . It only gets more fascinating. Check out the Mnx gene in this critter.

The Mnx (aka HB9) gene​

The Trichoplax Mnx sequence: ABC86118
Comparison of this sequence with a few others: Cladogram

The human Mnx1 gene.
The fly Mnx gene (exex)
The Zebrafish Mnx gene

What does it do?
It is involved in the development of the pancreas and motor neurons.
1) Zebrafish mnx genes in endocrine and exocrine pancreas formation.
2) The Mnx homeobox gene class defined by HB9, MNR2 and amphioxus AmphiMnx.

The HB9 homeobox gene has been cloned from several vertebrates and is implicated in motor neuron differentiation. In the chick, a related gene, MNR2, acts upstream of HB9 in this process. Here we report an amphioxus homologue of these genes and show that it diverged before the gene duplication yielding HB9 and MNR2. AmphiMnx RNA is detected in two irregular punctate stripes along the developing neural tube, comparable to the distribution of 'dorsal compartment' motor neurons, and also in dorsal endoderm and posterior mesoderm. We propose a new homeobox class, Mnx, to include AmphiMnx, HB9, MNR2 and their Drosophila and echinoderm orthologues; we suggest that vertebrate HB9 is renamed Mnx1 and MNR2 be renamed Mnx2.

Interesting research:​

Directed Evolution of Motor Neurons from Genetically Engineered Neural Precursors.

Stem cell-based therapies hold therapeutic promise for degenerative motor neuron diseases such as amyotrophic lateral sclerosis and for spinal cord injury. Fetal neural progenitors present less risk of tumor formation than embryonic stem (ES) cells but inefficiently differentiate into motor neurons, in line with their low expression of motor neuron-specific transcription factors and poor response to soluble external factors. To overcome this limitation, we genetically engineered fetal rat spinal cord neurospheres to express the transcription factors HB9, Nkx6.1 and Ngn2. Enforced expression of the three factors rendered neural precursors responsive to sonic hedgehog and retinoic acid and directed their differentiation into cholinergic motor neurons that projected axons and formed contacts with co-cultured myotubes. When transplanted in the injured adult rat spinal cord, a model of acute motor neuron degeneration, the engineered precursors transiently proliferated, colonized the ventral horn, expressed motor neuron-specific differentiation markers and projected cholinergic axons in the ventral root. We conclude that genetic engineering can drive the differentiation of fetal neural precursors into motor neurons which efficiently engraft in the spinal cord. The strategy thus holds promise for cell replacement in motor neuron and related diseases.

What did these guys do? They enforced the expression of 3 genes associated with neuronal development in order to direct the development of motor neurons. Sonic hedgehog also played a role .
So four genes played a role:

1. HB9
2. Nkx6.1
3. Ngn2
4. Sonic hedgehog

Are similar genes present in the Trichoplax genome?
1. HB9 (mnx)
Yes (see above).

2. Nkx6.1
Here is the human Nk6 gene
And here is the Trichoplax version

3. Ngn2
Here is the human neurogenin 2 (ngn2) gene
And here is the Trichoplax version.
A quick BLAST (blastp) the human genome shows this sequence to be closely related to ngn2 (E-value = 3^-8).

4. Sonic hedgehog (shh)
Here is the human shh gene
This gene seems to absent in from the Trichoplax genome, however, the presence of shh in Monosiga brevicollis (unicellular eukaryote that diverged before Trichoplax) suggest the possibility of gene loss in this lineage.

Wonder what will happen if shh is co-expressed and together with mnx, Nk6 and ngn2 in Trichoplax, or whether these genes will function like their counterparts in higher animals.

A complex array of neurologically associated developmental pathways present in this eumetazoan that has no nerves, sensory cells and muscle cells, and there is more .​

 

[Phronesis]

Another Hox gene in the Trichoplax genome involved in central nervous system development.

Hmx
Its function:
Hmx homeobox gene function in inner ear and nervous system cell-type specification and development.

The Hmx homeobox gene family is comprised of three members in mammals, Hmx1, Hmx2, and Hmx3, which are conserved across the animal kingdom and are part of the larger NKL clustered family of homeobox genes. Expression domains of Hmx genes in distantly related species such as Drosophila and mouse suggest an ancestral function in rostral central nervous system development. During vertebrate evolution, the Hmx genes appear to have been recruited into additional roles in inner ear morphogenesis and specification of vestibular inner ear sensory and supporting cell types. Being derived from a common ancestor, the vertebrate Hmx gene family is thus a strong candidate to investigate functional overlap versus the unique roles played by multiple genes belonging to the same family. The functions of Hmx2 and Hmx3 were investigated via directed gene mutagenesis and the primary regions where Hmx2 and Hmx3 exert their individual functions are consistent with their expression domains, such as the vestibule and uterus. Meanwhile, it is notable that some tissues where both Hmx2 and Hmx3 are extensively expressed were not severely affected in either of the Hmx2 or Hmx3 single mutant mice, suggesting a possible functional overlap existing between these two genes. Compound Hmx2 and Hmx3 double mutant mice showed more severe defects in the inner ear than those displayed by either single knockout. Furthermore, novel abnormalities in the hypothalamic-neuroendocrine system, which were never observed in either of the single mutant mice, confirmed a hypothesis that Hmx2 and Hmx3 also function redundantly to control embryonic development of the central nervous system.

The Trichoplax Hmx sequence. BLAST it.

Where is this critter's brain ? Did its mind get lost somewhere along the line, or is it just ready for a bit of cooption here and there ?

 

[Phronesis]

More preadaptations from Trichoplax:

The Hex Homeobox gene​

Its function?
Critical element in the development of the liver:
The role of Hex in hemangioblast and hematopoietic development.
The homeoprotein Hex is required for hemangioblast differentiation.
The homeobox gene HEX regulates proliferation and differentiation of hemangioblasts and endothelial cells during ES cell differentiation.

Detoxification of free radicals and damaging molecules play a crucial part in cellular homeostasis as well as systems homeostasis. The liver is mainly responsible for system homeostasis as it contains the highest concentration cells (hepatocytes do the heavy lifting) capable of detoxification, modification and excretion of hazardous molecules. It would be interesting to see what a gene that is associated with the development of the liver is doing in this simple organism at the base of the eumetazoan tree.

http://www.nature.com/nature/journal/v454/n7207/fig_tab/nature07191_T1.html​

http://www.nature.com/nature/journal/v454/n7207/fig_tab/nature07191_T1.html

And the Dbx gene?​

The trend of neurologically associated homeobox genes continues.
Regulation and function of Dbx genes in the zebrafish spinal cord.

Dbx homeodomain proteins are important for spinal cord dorsal/ventral patterning and the production of multiple spinal cord cell types. We have examined the regulation and function of Dbx genes in the zebrafish. We report that Hedgehog signaling is not required for the induction or maintenance of these genes; in the absence of Hedgehog signaling, dbx1a/1b/2 are expanded ventrally with concomitant increases in postmitotic neurons that differentiate from this domain. Also, we find that retinoic acid signaling is not required for the induction of Dbx expression. Furthermore, we are the first to report that knockdown of Dbx1 function causes a dorsal expansion of nkx6.2, which is thought to be the cross-repressive partner of Dbx1 in mouse. Our data confirm that the dbx1a/1b/2 domain in zebrafish spinal cord development behaves similarly to amniotes, while extending knowledge of Dbx1 function in spinal cord patterning. 2007 Wiley-Liss, Inc

 

[Phronesis]

Pitx: Another neurologically associated Hox gene present in the Trichplax genome.​

The various versions:
Trichoplax. Function unknown at present. Would be interesting to find out what it is.
Human Pitx1 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. Members of this family are involved in organ development and left-right asymmetry. This protein acts as a transcriptional regulator involved in basal and hormone-regulated activity of prolactin.

Human Pitx2 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. The encoded protein acts as a transcription factor and regulates procollagen lysyl hydroxylase gene expression. This protein plays a role in the terminal differentiation of somatotroph and lactotroph cell phenotypes, is involved in the development of the eye, tooth and abdominal organs, and acts as a transcriptional regulator involved in basal and hormone-regulated activity of prolactin. Mutations in this gene are associated with Axenfeld-Rieger syndrome, iridogoniodysgenesis syndrome, and sporadic cases of Peters anomaly. A similar protein in other vertebrates is involved in the determination of left-right asymmetry during development. Alternatively spliced transcript variants encoding distinct isoforms have been described

Human Pitx3 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. Members of this family act as transcription factors. This protein is involved in lens formation during eye development. Mutations of this gene have been associated with anterior segment mesenchymal dysgenesis and congenital cataracts.

Zebrafish Pitx1
Zebrafish Pitx2
Zebrafish Pitx3
Drosophila Ptx1 (fruitfly)

More interesting facts about Pitx:
The Pitx homeobox gene in Bombyx mori: Regulation of DH-PBAN europeptide hormone gene expression

The diapause hormone-pheromone biosynthesis activating neuropeptide gene, DH-PBAN, is expressed exclusively in seven pairs of DH-PBAN-producing neurosecretory cells (DHPCs) on the terminally differentiated processes of the subesophageal ganglion (SG). To help reveal the regulatory mechanisms of cell-specific DH-PBAN expression, we identified a cis-regulatory element that regulates expression in DHPCs using the recombinant AcNPV-mediated gene transfer system and a gel-mobility shift assay. Bombyx mori Pitx (BmPitx), a bicoid-like homeobox transcription factor, binds this element and activates DH-PBAN expression. The BmPitx was expressed in various tissues, including DHPCs in the SG. Suppression of DH-PBAN expression by silencing of the BmPitx successfully induced non-diapaused eggs from a diapause egg producer. To the best of our knowledge, this report is the first to identify a neuropeptide-encoding gene as a target of the Pitx transcriptional regulator in invertebrates. Thus, it is tempting to speculate that functional conservation of Pitx family members on neuropeptide gene expression occurs through a "combinational code mechanism" in both vertebrate and invertebrate in neuroendocrine systems.

PITX genes are required for cell survival and Lhx3 activation
Zebrafish pitx3 is necessary for normal lens and retinal development.

And the trend of neurologically associated genes present in this basal eumetazoan continues.....​

 

[Phronesis]

Otp: The trend of neurolically associated developmental genes in the genome of the Trichoplax continues...​

The various versions:
Trichoplax: Function unknown at present. Interested in its function in a basal eumetazoan.
Human otp. Its function:
The role of Otx and Otp genes in brain development.

Over the last ten years, many genes involved in the induction, specification and regionalization of the brain have been identified and characterized at the functional level through a series of animal models. Among these genes, both Otx1 and Otx2, two murine homologues of the Drosophila orthodenticle (otd) gene which encode transcription factors, play a pivotal role in the morphogenesis of the rostral brain. Classical knock-out studies have revealed that Otx2 is fundamental for the early specification and subsequent maintenance of the anterior neural plate, whereas Otx1 is mainly necessary for both normal corticogenesis and sense organ development. A minimal threshold of both gene products is required for correct patterning of the fore-midbrain and positioning of the isthmic organizer. A third gene, Orthopedia (Otp) is a key element of the genetic pathway controlling development of the neuroendocrine hypothalamus. This review deals with a comprehensive analysis of the Otx1, Otx2 and Otp functions, and with the possible evolutionary implications suggested by the models in which the Otx genes are reciprocally replaced or substituted by the Drosophila homologue, otd.

The same for mice:
The murine Otp homeobox gene plays an essential role in the specification of neuronal cell lineages in the developing hypothalamus.

Hypothalamic nuclei, including the anterior periventricular (aPV), paraventricular (PVN), and supraoptic (SON) nuclei strongly express the homeobox gene Orthopedia (Otp) during embryogenesis. Targeted inactivation of Otp in the mouse results in the loss of these nuclei in the homozygous null neonates. The Otp null hypothalamus fails to secrete neuropeptides somatostatin, arginine vasopressin, oxytocin, corticotropin-releasing hormone, and thyrotropin-releasing hormone in an appropriate spatial and temporal fashion, and leads to the death of Otp null pups shortly after birth. Failure to produce these neuropeptide hormones is evident prior to E15.5, indicating a failure in terminal differentiation of the aPV/PVN/SON neurons. Absence of elevated apoptotic activity, but reduced cell proliferation together with the ectopic activation of Six3 expression in the presumptive PVN, indicates a critical role for Otp in terminal differentiation and maturation of these neuroendocrine cell lineages. Otp employs distinct regulatory mechanisms to modulate the expression of specific molecular markers in the developing hypothalamus. At early embryonic stages, expression of Sim2 is immediately downregulated as a result of the absence of Otp, indicating a potential role for Otp as an upstream regulator of Sim2. In contrast, the regulation of Brn4 which is also expressed in the SON and PVN is independent of Otp function. Hence no strong evidence links Otp and Brn4 in the same regulatory pathway. The involvement of Otp and Sim1 in specifying specific hypothalamic neurosecretory cell lineages is shown to operate via distinct signaling pathways that partially overlap with Brn2.

The Zebrafish version. Its function: More of the same.
Differential regulation of the zebrafish orthopedia1 gene during fate determination of diencephalic neurons

The homeodomain transcription factor Orthopedia (Otp) is essential in restricting the fate of multiple classes of secreting neurons in the neuroendocrine hypothalamus of vertebrates. However, there is little information on the intercellular factors that regulate Otp expression during development

In the sea urchin.
Evolution of OTP-independent larval skeleton patterning in the direct-developing sea urchin, Heliocidaris erythrogramma.

The Orthopedia gene (Otp) encodes a homeodomain transcription factor crucial in patterning the larval skeleton of indirect-developing sea urchins.

A clear example of a cooption, whereby the same gene plays a role in neurological development in vertebrates and skeletal development in the sea urchin. Recycling of pre-existing genes for various, distinct, developmental processes.

 

[Phronesis]

Awesome articles:

Development Puts An End To Evolution Of Endless Forms​

ScienceDaily (Oct. 25, 2008) — Researchers have put forward a simple model of development and gene regulation that is capable of explaining patterns observed in the distribution of morphologies and body plans (or, more generally, phenotypes).

The study, by Elhanan Borenstein of the Santa Fe Institute and Stanford University and David Krakauer of the Santa Fe Institute was published in this month's issue of PLoS Computational Biology.

Nature truly displays a bewildering variety of shapes and forms. Yet, with all its magnificence, this diversity still represents only a tiny fraction of the endless 'space' of possibilities, and observed phenotypes actually occupy only small, dense patches in the abstract phenotypic space.[/B] Borenstein and Krakauer demonstrate that the sparseness of variety in nature can be attributed to the interactions between multiple genes and genetic controls involved in the development of organisms – a much simpler explanation than previously suggested.

Borenstein and Krakauer further integrated their model with phylogenetic dynamics, allowing developmental plans to evolve over time. They showed that this hybrid developmental-phylogenetic model reproduces patterns that are observed in the fossil record, including increasing variation between taxonomic groups, accompanied by decreasing variation within groups. This pattern is consistent with the Cambrian radiation associated with a rapid proliferation of highly disparate, multicellular animals, and suggests that much of the variation seen today is as a result of simpler genetic controls dating from much earlier in evolutionary time.

These simpler genetic controls include hox genes that are responsible for body plans, nervous systems, eyes etc. As seen, many of these switches were present in animals at the base of the evolutionary tree without any of these body plans, nervous system or eyes etc.

The article continues...

The findings presented in this study also bear directly on issues of convergence (when very different organisms independently evolve similar features). By including a model of development, rather different genotypes can produce very similar phenotypes. Consequently, convergent evolution, which the vast space of genotypes would suggest to be rare, is allowed to become much more common.

One of the paradoxical implications of this study has been to show how innovations in development that lead to an overall increase in the number of accessible phenotypes, can lead to a reduction in selective variance. In other words, while the potential for novel phenotypes increases, the fraction of space these phenotypes occupies tends to contract.

They concluded that "The theory presented in our paper complements the view of development as a key component in the production of endless forms and highlights the crucial role of development in constraining (as well as generating) biotic diversity."

And there we have it... biasing (constraining) of evolutionary trends as a result of genetic information present in simpler genetic controls dating from the base of the evolutionary tree (preadaptations).

The free, online peer-reviewed article:

An End to Endless Forms: Epistasis, Phenotype Distribution Bias, and Nonuniform Evolution​

These findings complement the view of development as a key component in the production of endless forms and highlight the crucial role of development in constraining biotic diversity and evolutionary trajectories.

The role of development in generating, or constraining, biotic diversity has been one of the most active debates in evolutionary biology [32]–[34]. The roots of this debate go back to the study of homologies and questions over physico-chemical verses genetically-selected rules of growth. One merit of simple developmental models is to illustrate how these two positions reflect necessary, complementary properties of generic developmental programs. Regulatory epistasis introduces non-linearities into development, allowing similar genotypes to generate significant divergence among phenotypes, whereas degeneracy tends to contract the occupancy of morphospace and bias phenotypic samples. Of great interest is how these structural properties of development have themselves been modified over the course of evolutionary time, potentially changing the tempo and mode of the evolutionary process. One of the paradoxical implications of this study has been to show how innovations in development (arising through increasing regulatory dimensions) that lead to an increase in the volume of accessible phenotypes, can lead to a reduction in selective variance (through increasing regulatory epistasis), so whereas the potential for novel phenotypes increases, the fraction of space these phenotypes occupies tends to contract. Hence the evolutionary process moves from a macro-configuration, sampling distant regions of space sparsely, to a micro configuration, sampling local regions of space at high resolution. This is analogous to an annealing process, whereby as an optimization process proceeds, the solutions become more frequent and more densely localized around the putative solution points.

This is analogous to evolution being a memetic algorithm (nice paper discussing it) with a set fitness function in a pre-existing fitness landscape. Convergence is to be expected.

Take the following into consideration:

• Evolution is constrained (biased) as a result of genetic information present in simpler genetic controls dating from the base of the evolutionary tree (preadaptations)..
• We observe many preadaptations for multicellularity in primitive unicellular organisms.
• Also several toolkits (also preadaptations) for the development of body plans (Hox genes), the nervous system and sensory organs in animals at the base of the eumetazoan tree.
• Also, spectacular examples of convergence are observed in nature.

How do stem cells become specialized?
Many Paths, Few Destinations: How Stem Cells Decide What They'll Become

How does a stem cell decide what specialized identity to adopt -- or simply to remain a stem cell? A new study suggests that the conventional view, which assumes that cells are "instructed" to progress along prescribed signaling pathways, is too simplistic. Instead, it supports the idea that cells differentiate through the collective behavior of multiple genes in a network that ultimately leads to just a few endpoints -- just as a marble on a hilltop can travel a nearly infinite number of downward paths, only to arrive in the same valley.

 

[Phronesis]

On the development of eyes​

Several types of eyes exist and these include the camera-type eye, the compound eye, and the mirror eye (Figure 1). Ernst Mayr proposed that eyes evolved in all animal phyla 40 to 60 times independently.
A monophyletic program governing the development of the different eye types is proposed and the Pax6 gene is posited to be the master control gene. The Pax6 gene also plays a part in controlling the development of the nose, ears and parts of the brain.

What is needed for the developmental program of eyes?
A few core genes include:
Pax6 (eyeless [eye]) in Drosophila)
Six-type genes (E.g. Six3)
Sox-type genes (E.g. Sox2)
atonal ( E.g. Atoh7)
Retinoid receptors
Fox transcription factors (E.g. FoxN4)
Pitx

Fascinating experiments have been conducted by shuffling around the genetic program architecture of genes associated with eye development in various animals.
For example in Drosophila:
Ectopic eye structures are able to be induced on the antennae, legs, and wings of fruit flies. This is done by targeted expression of the eyeless gene (Pax6 Drosophila homologue) (Figure 2). The Pax6 gene from the mouse is able to do the same job as the Drosophila version (Figure 3). And in Xenopus embryos, ectopic eye structures in can also be induced by the Drosophila eyeless (Pax6) version (Figure 4).

What about the Trichoplax adhaerens genome? Any genes for eye development?
It seems quite a chunk of the circuitry needed for eye development is present. (From table 1)
PaxB (eyeless?)
Six genes
Sox gene
Atonal gene
Retinoid X Receptor
Fox transcription factors
Pitx

All that is missing seems to be crystalins (plays a part in lens formation). However, Darwin posited that "The simplest organ which can be called an eye consists of an optic nerve, surrounded by pigment-cells and covered by translucent skin, but without any lens or other refractive body." Thus large chunks of the circuitry for eye development in Trichoplax is present but no eyes!

Now compare the developmental program to evolution.
Here is an interesting article that shows the parallels between evolution and development.

For development:
Primordial germ cells (PGC) are prevented from entering the somatic program and are demethylated (genome-wide erasure of existing epigenetic modifications). Then the gametes are imprinted (targeted DNA methylation) during gametogenesis, only to be demethylated again after fertilization. Then during development, DNA is methylated again, causing totipotential cells to become pluripotent. X-inactivation and reactivation (of the paternal gamete I think) also occurs. The whole process is governed by the genetic (and epigenetic?) program. During the unfolding of this somatic program, random variation and selection occur, ultimately leading to just a few endpoints, every time it is successful. The process is constrained (few end points) as a result of pre-existing information that is set up during the inititiation of the process. All this is controlled by information in the genome.

For evolution:
There also seems to be only a few endpoints (small subset, limited variation) out of all the possible endpoints.
In the article:
An End to Endless Forms: Epistasis, Phenotype Distribution Bias, and Nonuniform Evolution
It is argued to be as a result of genetic instructions dating earlier in evolutionary time. Preadaptations...

As already seen in the evolution of eyes, as soon as these sets of genes were formed (E.g. Pax genes), through whatever mechanism), evolution seemed to have been biased to a few end points, and these few endpoints arose 40-60 times, independently, as a result of pre-existing (preadaptations) information in the case of eyes.

What other "biased" end points can there be? Nervous systems, smell, hearing? And why would evolution be biased, as in development, to only reach a few end points over and over?

 

[Phronesis]

Evolution seems to be biased towards a few endpoints. This is partly due to the massive amounts of preadaptations in organisms at the base of the evolutionary tree. Now evolution seems to learn....

Facilitated Variation: How Evolution Learns from Past Environments To Generalize to New Environments
Abstract:

One of the striking features of evolution is the appearance of novel structures in organisms. Recently, Kirschner and Gerhart have integrated discoveries in evolution, genetics, and developmental biology to form a theory of facilitated variation (FV). The key observation is that organisms are designed such that random genetic changes are channeled in phenotypic directions that are potentially useful. An open question is how FV spontaneously emerges during evolution. Here, we address this by means of computer simulations of two well-studied model systems, logic circuits and RNA secondary structure. We find that evolution of FV is enhanced in environments that change from time to time in a systematic way: the varying environments are made of the same set of subgoals but in different combinations. We find that organisms that evolve under such varying goals not only remember their history but also generalize to future environments, exhibiting high adaptability to novel goals. Rapid adaptation is seen to goals composed of the same subgoals in novel combinations, and to goals where one of the subgoals was never seen in the history of the organism. The mechanisms for such enhanced generation of novelty (generalization) are analyzed, as is the way that organisms store information in their genomes about their past environments. Elements of facilitated variation theory, such as weak regulatory linkage, modularity, and reduced pleiotropy of mutations, evolve spontaneously under these conditions. Thus, environments that change in a systematic, modular fashion seem to promote facilitated variation and allow evolution to generalize to novel conditions.

Biased evolution towards a few endpoints under intrinsic control.

 

[Phronesis]

Rolling 'Sea Grape' Rocks The Fossil Record

ScienceDaily (Dec. 4, 2008) — A submarine expedition that went looking for visually flashy sea creatures instead found a drab, mud-covered blob that may turn out to be truly spectacular indeed.

Hopefully someone will sequence the genome of this interesting little critter .

Genetic Patterning In Fruit Fly Development Identified

ScienceDaily (Dec. 1, 2008) — No matter the species, from flies to humans, we all start the same: a single-cell fertilized egg that embarks on an incredible journey. The specifics of this journey are being uncovered at Rutgers University-Camden, where a biologist is researching how from one cell a jumble of many are able to organize and communicate, allowing life to spring forth.

See if you can spot the similarities between evolution and development.

The new Developmental Cell article offers precise outcomes for the tens of genes and hundreds of patterns involved in four developmental stages of the fruit fly’s eggs. As part of a research team, Yakoby developed an innovative new coding language to formally follow and manage the dynamics of hundreds of gene-patterns. The team concentrated on the two main patterning pathways of the Drosophila egg development: bone morphogenetic protein and epidermal growth factor receptor. Most developmental and other diseases, such as cancer, are associated with these universal pathways.

Just like embryos, animals at the base of the evolutionary tree had a plethora of information available to develop eyes, nervous system, body plans etc... Mmmm.

 

[Phronesis]

Two-phase increase in the maximum size of life over 3.5 billion years reflects biological innovation and environmental opportunity.

The maximum size of organisms has increased enormously since the initial appearance of life >3.5 billion years ago (Gya), but the pattern and timing of this size increase is poorly known. Consequently, controls underlying the size spectrum of the global biota have been difficult to evaluate. Our period-level compilation of the largest known fossil organisms demonstrates that maximum size increased by 16 orders of magnitude since life first appeared in the fossil record. The great majority of the increase is accounted for by 2 discrete steps of approximately equal magnitude: the first in the middle of the Paleoproterozoic Era (1.9 Gya) and the second during the late Neoproterozoic and early Paleozoic eras (0.6–0.45 Gya). Each size step required a major innovation in organismal complexity—first the eukaryotic cell and later eukaryotic multicellularity. These size steps coincide with, or slightly postdate, increases in the concentration of atmospheric oxygen, suggesting latent evolutionary potential was realized soon after environmental limitations were removed.

So life on earth is preadapted for future climate scenarios to adequately adjust to changes....mmm.

Although increase in maximum size over time can often be accounted for by simple diffusive models (18, 29, 30), a single diffusive model does not appear capable of explaining the evolution of life’s overall maximum size. Approximately 3/4 of the 16-orders-of-magnitude increase in maximum size occurred in 2 discrete episodes. The first size jump required the evolution of the eukaryotic cell, and the second required eukaryotic multicellularity. The size increases appear to have occurred when ambient oxygen concentrations reached sufficient concentrations for clades to realize preexisting evolutionary potential, highlighting the long-term dependence of macroevolutionary pattern on both biological potential and environmental opportunity.

Preexisting evolutionary potential? Sounds like the necessary information to react to different environments was already present in organism in order to respond to various environment. Nice preadaptations, no need for random inventions, just the unfolding of latent potential with the use of evolutionary processes (RV+NS).

 

[alloytoo]

Two-phase increase in the maximum size of life over 3.5 billion years reflects biological innovation and environmental opportunity.

So life on earth is preadapted for future climate scenarios to adequately adjust to changes....mmm.




Preexisting evolutionary potential? Sounds like the necessary information to react to different environments was already present in organism in order to respond to various environment. Nice preadaptations, no need for random inventions, just the unfolding of latent potential with the use of evolutionary processes (RV+NS).

Real scientists, you know the one's in a lab, doing research, etc etc disagree with you and Uncommon Descent. You know these folks at uncommon descent don't really do any lab work, any research, perhaps by your standards they should well refrain from commenting on science (since they envariably get it wrong anyway).

 

[Phronesis]

Real scientists, you know the one's in a lab, doing research, etc etc disagree with you and Uncommon Descent. You know these folks at uncommon descent don't really do any lab work, any research, perhaps by your standards they should well refrain from commenting on science (since they envariably get it wrong anyway).

It would be nice if you could discuss what they disagree with. As to the people at uncommondescent, I don't know their qualifications.

But feel free to add information regarding preadaptations (the purpose of this thread ).

Remember Trichoplax? Eukaryote at the base of the eumetazoan tree with only four cell types. Well, this animal has no nervous system, look at the function of the gene present in this animal's genome.

POU class 4 (Brn-3)​

Developmental expression of the POU domain transcription factor Brn-3b (Pou4f2) in the lateral line and visual system of zebrafish.

Members of the class IV POU domain transcription factors are important regulators of neural development. In mouse, Brn-3b (Pou4f2, Brn3.2) and Brn-3c (Pou4f3, Brn3.1) are essential for the normal differentiation and maturation of retinal ganglion cells (RGCs) and hair cells of the auditory system, respectively. In this report, the cloning and expression profile of brn-3b in the zebrafish (Danio rerio) were assessed as the first step for understanding its role in the development of sensory systems. Two brn-3b alternative transcripts exhibited different onset of expression during development but shared overlapping expression domains in the adult visual system. The brn-3b expression in the zebrafish retina was consistent with a conserved role in differentiation and maintenance of RGCs. Expression was also observed in the optic tectum. Unexpectedly, brn-3b was prominently expressed in the migrating posterior lateral line primordium and larval neuromasts. For comparison, brn-3c expression was limited to the otic vesicle and was not detected in the lateral line during embryonic development. The expression of brn-3b in the mechanosensory lateral line of fish suggests a conserved function of a class IV POU domain transcription factor in sensory system development.

Placodal origin of Brn-3-expressing cranial sensory neurons.

The Brn-3 class of POU-domain transcription factors includes three genes in mammals which have key roles in the development of specific groups of sensory neurons. Here, we have identified three avian genes which correspond to the murine genes Brn-3.0, Brn-3.1, and Brn-3.2. Using an in situ hybridization probe generic for this gene class, the earliest detectable expression of Brn-3 in the chick is at stage 15, in placodal and migrating precursors of the trigeminal ganglion. By stage 19, Brn-3.0 protein is detectable in the trigeminal and vestibulocochlear ganglia with Brn-3.0-specific antisera, and Brn-3 message expression has extended to the dorsal root ganglia. At later stages, when condensation of the trigeminal ganglion is complete, Brn-3.0-immunoreactive neurons are concentrated in the portion of the ganglion distal to the brain stem. To examine the developmental origin of the Brn-3 expressing cells, we combined lipophilic dye (DiI) labeling with in situ hybridization. DiI labeling of the placodal surface ectoderm and of premigratory neural crest cells in the neural tube reveals that all, or nearly all, of the Brn3-expressing neurons in the trigeminal ganglia are derived from the sensory placodes and not from the neural crest, and thus, that Brn-3 is an early marker of the placode-derived sensory neural lineage.

Looks like neurons were inevitable...

 

[alloytoo]

It would be nice if you could discuss what they disagree with. As to the people at uncommondescent, I don't know their qualifications.

Riiiiiiight.....I believe.........

Random mutation and natural selection. No preplanning, not even on a cellular level. Them little cells don't have minds remember.

But feel free to add information regarding preadaptations (the purpose of this thread ).

I thought the purpose of this thread was to push your deceitful creationist agenda.

My bad.